There's nothing like hearing the results of studies directly from those who actually conducted the research. In this interview, you'll meet one of these impressive HIV researchers and read his explanation of a study he presented at CROI 2009.

My name's Jason Baker. I'm from the University of Minnesota, and I head up the county medical center in Minneapolis, Minnesota.

What we did in this study was enroll a prospective cohort of patients, both HIV-infected and HIV-negative, and have them come in for one visit to assess their vessel function and some inflammatory markers.1

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We did this to look at HIV infection independent of antiretroviral therapy. We studied 32 untreated HIV-infected patients, and compared them to HIV-negative patients who did not differ with respect to age, gender, race, ethnicity, blood pressure and BMI [Body Mass Index.]. There were very few patients with diabetes -- only two. Use of statins or lipid lowering agents was infrequent.

There were differences seen, with more injection drug use and hepatitis C in the HIV-infected group, and a potential trend towards more smokers. But smoking was over represented in both.

These HIV-infected patients had high T-cells, median value of 391, with viral levels up around 10,000, consistent with not receiving antiretroviral therapy. About 85 percent of the HIV-infected patients were naïve to therapy, with the remaining few patients having received treatment more than two years back.

Comparing the two groups, there were elevated IL-6 d-dimer levels in the HIV-infected group. We assessed their radial artery diastolic pulse contour that's a function through pulse-wave analysis, analyzing the diastolic portion of the curve, which gives us an assessment of both large-vessel elasticity and small-vessel elasticity -- both of which are markers of cardiovascular risk.

Both the large- and the small-vessel elasticity were impaired with HIV infection, compared to the uninfected group. This difference persisted after adjustment for Framingham risk score. Some of the factors that were different in the demographics would be injection drug use, HDL, smoking status, and we also adjusted for age in that model.

Then we did a fully adjusted model: age, gender, race, ethnicity, hepatitis C and HDL, and there was still a significant impairment of both large and small arterial elasticity.

Finally, we took the small arterial elasticity and correlated it with d-dimer, and it was a significant inverse correlation, showing that with elevated d-dimer levels, the small-vessel elasticity was impaired. This is consistent with the thought that most of the vessel surface area is out at the periphery and the microcirculation, and so dysfunction of endothelial surfaces at that level would be important for inflammatory or increased thrombotic activity.

So these measures cannot only help us assess cardiovascular risk, but give us something to track adjunct interventions, to try to decrease inflammation and decrease thrombotic activity.

I see in your discussion, you're suggesting that these methods might be a good way to assess this in HIV-infected patients. Are you using it at the clinic?

We're not using it clinically; we're doing it for research purposes. There are a lot of ways to assess vessel dysfunction, and this is just one.

I think the advantages are it assesses both the large vessels and the small vessels, and it's reproducible. So, looking to study this a little more before advocating clinical use, you want to do some multi-centered studies where you have something that's repeatable within different operators and within the same patient over time if nothing's changed.

We're looking towards trying to get funding to do this in multi-centered studies, to look at the effects of starting treatment on vessel function, look at the effects of anti-inflammatory treatments in HIV-positive patients to further decrease their risk for heart disease, This is particularly important because HIV-positive patients are living longer and doing better on therapy. So the whole point is we may need to think about adjunct treatments to further reduce their heart disease risk, and this might be a way to assess that. It provides an assessment of early disease, before people go on to have heart attacks and events; we'd like to detect it early so that we can change their risk early.

I see a very large percentage of the HIV-infected population was smokers -- 59 percent. Usually the number is more like 40. Did you account for that?

Yes. In general, in HIV-infected patients there tend to be more smokers, compared to the general population. In the general population, the rate is probably 25 percent. We had 59 percent in our HIV-infected group, 40 percent in our HIV-negative group, but when we adjusted for smoking status, the differences in elasticity between the two groups persisted.

What percentage had a prior AIDS diagnosis?

Sixteen percent, five of the 32 patients who were HIV infected had a prior AIDS diagnosis. That didn't seem to predict elasticity. So comparing those with an AIDS diagnosis to the patients who didn't have this diagnosis. didn't seem to effect that.

This article was provided by TheBodyPRO.com. It is a part of the publication The 16th Conference on Retroviruses and Opportunistic Infections.

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